Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

NBXFO hybridoma cells produced both the membrane and secreted isoforms of macrophage colony-stimulating factor (M-CSF). Murine bone marrow cells stimulated by the secreted form of M-CSF (sM-CSF) became Mac1+, Mac2+, Mac3+, and F4/80+ macrophages that inhibited the growth of NBXFO cells, but not L1210 or P815 tumor cells. In cytotoxicity studies, M-CSF activated macrophages and freshly isolated macrophages killed NBXFO cells in the presence of polymyxin B, eliminating the possibility that contaminating lipopolysaccharide (LPS) was responsible for the delivery of the cytotoxic signal. Retroviral-mediated transfection of T9 glioma cells with the gene for the membrane isoform of M-CSF (mM-CSF), but not for the secreted isoform of M-CSF, transferred the ability of macrophages to kill these transfected T9 cells in a mM-CSF dose-dependent manner. Macrophage-mediated killing of the mM-CSF transfected clone was blocked by using a 100-fold excess of recombinant M-CSF. Catalase, superoxide dismutase, and the nitric oxide inhibitor, N-omega-nitro-arginine methyl ester (NAME), did not effect macrophage cytotoxicity against the mM-CSF transfectant T9 clones. T9 parental cells when cultured in the presence of an equal number of the mM-CSF transfectant cells were not killed, indicating specific target cell cytotoxicity by the macrophages. Electron microscopy showed that macrophages were capable of phagocytosizing mM-CSF bearing T9 tumor cells and NBXFO hybridoma cells; this suggested a possible mechanism of this cytotoxicity. This study indicates that mM-CSF provides the necessary binding and triggering molecules through which macrophages can initiate direct tumor cell cytotoxicity.
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PMID:Macrophages can recognize and kill tumor cells bearing the membrane isoform of macrophage colony-stimulating factor. 865 38

We investigated the expression of granulocyte colony-stimulating factor (G-CSF), G-CSF mRNA, and G-CSF receptor mRNA in astrocytoma cell lines, G-CSF in astrocytoma cyst fluid, and the effect of recombinant G-CSF on the proliferation of astrocytoma cells in vitro and in vivo. We first examined supernatants from astrocytoma cell lines for the presence of G-CSF by ELISA. G-CSF was expressed by 6 of 14 astrocytoma cell lines constitutively, and, was detected after stimulation with tumor necrosis factor-alpha (TNF-alpha) in four of eight cell lines which did not produce G-CSF constitutively. G-CSF mRNA was detected by reverse-transcriptase polymerase chain reaction (RT-PCR) in all cell lines studied, suggesting that astrocytoma cells have the potential to produce G-CSF. We also analyzed the presence of G-CSF by ELISA in five astrocytoma cyst fluids. G-CSF was detected in one case. Although, in vitro study, the growth of glioma cells was not affected by rG-CSF, in a mouse model, the administration of G-CSF significantly shortened the time to tumor appearance and accelerated tumor growth. These data suggest that G-CSF has a stimulatory effect on the proliferation of astrocytoma cells in vivo through the mediation of host factors.
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PMID:Granulocyte colony-stimulating factor (G-CSF) production by astrocytoma cells and its effect on tumor growth. 869 23

Atrial natriuretic peptide (ANP) influences the activity of rat hypothalamic neurons, modifies the membrane excitability of the rat forebrain neurons, and induces changes in membrane potentials in cultured rat glioma cells. In order to explore whether these effects are reflected in the electrical activity of larger subcortical brain areas, we investigated the electroenceophalographic activity (EEG) recorded from 20 male albino (New Zealand White) rabbits. Recordings of EEG were made on restrained, conscious animals 1 week after the implantation of an indwelling intracerebroventricular (i.c.v.) cannula (lateral right ventricle) and two stainless steel electrodes, implanted in the paraventricular (PVN) and supraoptic (SON) nuclei. Animals were classified into two main groups: those with water available ad libitum (group A) and those which were dehydrated for 24 h before EEG recordings (group B). Each group was divided into two subgroups (1 and 2) of five animals each. EEG was recorded at 0 min (control) and 30, 60, and 90 min following the i.c.v. injection of either 25 microliters artificial cerebrospinal fluid (aCSF; subgroup 1) or 1 microgram alpha-human ANP in 25 microliters a CSF (subgroup 2). Each EEG record duration was 6 s. For each EEG record the power spectrum of the digitized waveform was estimated in the frequencies 0.5-48 Hz using the fast Fourier transform, and the energy of each waveform was subsequently calculated. The results were analyzed by repeated-measures ANOVA and by the t-test. The analysis revealed that (1) water deprivation does not affect mean EEG energy and value (2) ANP attenuates (P < 0.05; in comparison with zero time) the mean energy value of EEG recorded from SON at 30 min and 60 min in the frequencies 8-48 Hz, whilst it tends to decrease (P < 0.1) the mean energy of EEG recorded from PVN at 30 min in the frequencies 8-15 Hz. Mean EEG energy changes caused by ANP would reflect its various (mainly inhibitory) effects on the electrical activity recorded from PVN and SON neurons in in vitro and in vivo studies.
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PMID:Effects of intracerebroventricular administration of atrial natriuretic peptide on subcortical EEG activity in conscious rabbits. 880 Nov 22

A 21-year-old woman was diagnosed with Turcot's syndrome (TS) at age 16 years. She had two ependymomas, one was located in the left middle cerebellar peduncle and the other in the low sacral spinal canal. Her mother and brother both had colectomies for colonic polyposis. Her maternal uncle and grandfather also had this disease and both died from cancer of the colon in their fourth decade of life. The patient was found to have hyperpigmented spots in the retina, skull osteomas and normal neurological examinations. The bone scan and CSF were normal and she had a germline mutation in the segment 3 of the adenomatous polyposis coli (APC) gene. Following partial resection of the two ependymomas, she was treated with radiation and chemotherapy. One year after surgery, paraspinal desmoid tumors were found and removed. She is presently 42 months postsurgical resection of the neural tumors and has remained central nervous system tumor-free. The occurrence of multiple ependymoma in TS has not been reported, and the control of this patient's ependymomas is consistent with other reports of long-term survival with TS and glial tumors.
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PMID:Multiple ependymomas in a patient with Turcot's syndrome. 895 Mar 38

A series of 34 patients with tumours of the third ventricle were operated on by a transcallosal route. Basal extrinsic lesions compressing or invading the ventricle as well as tumours located in the pineal area were excluded from this review. Tumours were approached by a transforaminal entry in 16 cases (47%), by an interforniceal route in 11 (32%), by a subchoroidal entry in 4 (14%) and by a combined transforaminal and subchoroidal entry in 3 (9%). Four out of 34 patients were submitted to a second operation, through the same approach corridor: 2 for an incomplete removal of an intrinsic tumour and 2 for a late regrowth. Postoperative mortality rate accounted for 5.8% (2 patients). Major post operative complications were hemiparesis (4 patients) and diabetes insipidus (4 patients), that were transient in 3. Akinetic mutism like status was observed in only 1 patient. Postoperative psychic disturbances were noticed in 5 cases. Nine out of 21 patients (62%) with preoperative hydrocephalus required a permanent CSF shunt. Histology revealed that 21 tumours (62%) were intraaxial (4 pilocitic astrocytoma, 10 low grade glioma, 1 giant cell astrocytoma, 1 subependymoma, 4 ependymoma/ependymoblastoma, 1 neurocitoma) and 13 (38%) were extraaxial (8 colloid cyst, 2 craniopharingioma, 1 ectopic pituitary adenoma, 1 lymphocytic hypophysitis and 1 metastasis). Total excision of third ventricle tumours was achieved in all patients with extraaxial tumours and in 62% and 71% of intraaxial tumours with the first and second surgical procedure respectively. Ten out of 34 patients of this series were submitted to a complete neuropsychological evaluation at an interval of 2-9 years after surgery. Memory tests were pathological in 2. Disconnection signs were constantly absent. Control function were preserved. Transcallosal approach remains the best microsurgical method of third ventricle tumours treatment. This route provides the capability for a superior visualization of the entire cavity of the third ventricle through different corridors. Permanent neurological and neuropsychological deficits are not frequent. Epilepsy, that accounted for 28% in patients submitted to transcortical transventricular approach to third ventricle tumours, was never noticed in this series operated on through a transcallosal route.
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PMID:Transcallosal approach to tumors of the third ventricle. Surgical results and neuropsychological evaluation. 927 58

Analysis of 139 CSF samples from living subjects, using iso-electric focusing in polyacrylamide gels, demonstrated an anomalous molecular form of acetylcholinesterase (AChE). This form was present in 84 of 87 patients with a clinical diagnosis of Alzheimer's disease (AD), 28 of whom have died and in whom histopathological confirmation of AD was obtained. The abnormal AChE form was also present in 22 of 23 patients with clinical dementia not regarded as AD type. In the six patients who died this abnormal AChE form was found in three cases of multi-infarct dementia, one with cerebral glioma with dementia and one with clinical dementia, but no pathology was found based on the Khachaturian criteria for AD. One patient with normal pressure hydrocephalus was negative when tested for the abnormal AChE form. This evidence indicates that the anomalous molecular form of AChE may not be specific for AD, and may possibly be a common indicator for organic dementia. The discovery of this form in 27 of 29 age-matched non-demented controls may indicate that the anomalous molecular form of AChE may not only exist in patients with clinically detectable dementia, but is probably present for a period before the onset of dementia. Recognizing and understanding the existence of pre-clinical dementia would be beneficial in designing a strategy for both the prevention and the treatment of dementia.
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PMID:An CSF anamalous molecular form of acetylcholinesterase in demented and non-demented subjects. 935 48

Progressive multifocal leukoencephalopathy is a subacute demyelinating disease of the central nervous system due to an opportunistic infection by a polyomavirus, most often JC virus, which predominantly infects oligodendrocytes. Progressive multifocal leukoencephalopathy used to be a rare condition, usually complicating lymphoproliferative diseases. Since the onset of the AIDS epidemic, its incidence has considerably increased and HIV infection has become, by far, the main risk factor for the disease. In AIDS patients, progressive leukoencephalopathy frequently shows atypical clinical and pathological features. The development of malignant glial tumors, within demyelinating regions, in patients with progressive multifocal leukoencephalopathy, has been reported in exceptional cases. The course of progressive multifocal leukoencephalopathy is invariably fatal. The diagnosis can only be made with certainty by histopathological examination of the brain, on cerebral biopsy or at postmortem. However, neuroradiological features may be extremely suggestive in many cases and PCR seems to be a reliable technique for demonstrating viral genome in the CSF. A few antiviral treatments have been proposed, however their efficacy is difficult to assess due to the low prevalence of the disease and the occurrence of rare cases with spontaneously prolonged survival.
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PMID:[Progressive multifocal leukoencephalopathy: virological and neuropathological aspects]. 938 4

Seventeen patients less than or equal to 20 years of age with newly diagnosed (n = 10) or recurrent (n = 7) malignant gliomas (anaplastic astrocytoma and glioblastoma multiforme) were treated with cyclophosphamide in association with hematopoietic cytokines (GM-CSF or G-CSF). Cyclophosphamide was given at a dose of 2 g/m2 daily for 2 days at 4-week intervals. Toxicity consisted of grade IV neutropenia and thrombocytopenia in 95% and 48% of cycles, respectively. There were no cyclophosphamide-related cardiac, pulmonary, or urothelial toxicities observed. Four of 10 patients with newly diagnosed disease demonstrated responses (three complete and one partial responses; one CR was only of 2 months duration). None of the seven patients with recurrent tumors demonstrated a response. We conclude that high-dose cyclophosphamide warrants further evaluation in children with newly diagnosed malignant glioma.
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PMID:Activity of high-dose cyclophosphamide in the treatment of childhood malignant gliomas. 940 13

Brain tumors have an immunoprivileged status which contributes to their refractoriness to treatment. In this study, immune rejection of GL261 glioma tumors in the mouse brain was achieved by subcutaneous vaccination with GM-CSF-transduced glioma cells. Cultured GL261 cells were transduced to secrete murine GM-CSF using a retrovirus vector, then irradiated, and injected subcutaneously into H-2 matched C57BL/6 mice. In prevaccination studies, the median survival time (MST) of animals vaccinated with 5 x 10(4) or 5 x 10(5) GM-CSF-transduced cells 7 days prior to intracranial injection of 10(6) nontransduced, nonirradiated GL261 cells was significantly prolonged by 45-50% compared with animals vaccinated in parallel with nontransduced, irradiated glioma cells. In treatment of established gliomas, the MST of animals, which were treated subcutaneously with 5 X 10(6) irradiated GM-CSF-transduced cells 3 days after intracranial injection of 2 x 10(4) nontransduced cells, was prolonged significantly by 36% compared with animals treated with the same number of nontransduced, irradiated cells or to sham-treated animals. In prevaccination studies, histology of brain tumors 4 days after intracranial tumor cell injection revealed infiltrates of CD8+ lymphocytes and eosinophils, the latter exclusively in animals vaccinated with GM-CSF-transduced cells, Thus, subcutaneous injection of irradiated GM-CSF-transduced glioma cells can induce a potent immune response to intracranial gliomas both as a vaccination against subsequent intracranial glioma cell implantation and for treatment of established intracranial glioma.
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PMID:Vaccination for experimental gliomas using GM-CSF-transduced glioma cells. 940 4

Rat T9 glioma cells transfected with the gene for the membrane isoform of macrophage-CSF (mM-CSF) but not for the secreted isoform of M-CSF were directly killed by bone marrow-derived macrophages. Macrophage-mediated cytolysis of the mM-CSF-transfected clone was blocked by using chemical inhibitors of phagocytosis such as iodoacetate, 2-deoxyglucose, gadolinium chloride, and cytochalasin B. In contrast, macrophage-mediated killing of mM-CSF-expressing tumor cells was augmented by the microtubule inhibitor, colchicine. Use of nitric oxide and reactive oxygen intermediate inhibitors failed to alter the macrophage-mediated killing of the mM-CSF-transfected tumor cells. Photomicroscopy, using immunohistochemical staining with the anti-Hck Ab to distinguish macrophages from tumor cells, revealed that phagocytosis began within 2 h after addition of the mM-CSF-bearing tumor cells. Photocinematography confirmed that macrophages first phagocytosized and then lysed the internalized mM-CSF transfectant cells. Using annexin V and acridine orange staining techniques, macrophages phagocytosized living mM-CSF-transfected tumor cells.
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PMID:Macrophages kill T9 glioma tumor cells bearing the membrane isoform of macrophage colony stimulating factor through a phagocytosis-dependent pathway. 955 92


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